In an article published online on June 24, 2009 in the American Journal of Clinical Nutrition, Scandinavian researchers report that young type 1 diabetic patients with higher vitamin C levels have better vascular function compared to those with lower levels of the vitamin. Vascular function and structure changes can occur early in type 1 diabetes, and are associated with a greater risk of cardiovascular disease and cardiovascular mortality later in life.

Petru Liuba and Michael Odermarsky of Lund University Hospital in Sweden, along with Jens Lykkesfeldt of the University of Copenhagen in Denmark, recruited 33 male and 26 female diabetic patients between the ages of 10 and 22 for the current study. Carotid intima-media thickness (cIMT, which measures atherosclerosis), assessments of cutaneous microvascular function, cardiac depolarization and repolarization (evaluated via electrocardiogram as QT interval corrected for heart rate, which, when prolonged, is a predictor of adverse cardiovascular prognosis), lipids, and plasma C-reactive protein, fibrinogen, vitamin C and oxidized vitamin C (dehydroascorbic acid) were assessed.

For subjects whose plasma vitamin C levels were among the lowest third of participants, carotid artery intima-media thickness and QT interval duration were greater than those whose vitamin C levels were in the highest third. Additionally, an assessment of cutaneous microvascular response was reduced in those whose vitamin C levels were lowest.

Oxidized vitamin C was found to increase as vitamin C levels decreased--a correlation that has been found in smokers. The finding suggests the presence of high oxidative stress levels in type 1 diabetes patients.

"It is not yet known whether vitamin C supplementation at a younger age could decelerate intimal thickening or retard the onset of cardiovascular complications in later life," the authors write. "On the basis of the epidemiologic evidence, this might be an important task for future studies given the predictive value of childhood cIMT in atherosclerosis progression and complications in the adult life."

There are two types of diabetes: type 1 and type 2. Underlying either form of diabetes is a disorder of insulin production, use, or both. Insulin is a hormone responsible for transporting glucose into cells. When there is excess glucose in the blood, insulin is secreted from the pancreas and signals the liver and muscles to store glucose as glycogen. Insulin also stimulates adipose tissue to store glucose as fat for long-term energy reserves. Insulin receptors are found in all cells throughout the body. In a healthy person, blood glucose levels are extremely stable (Kumar V et al 2005). Normal fasting glucose levels range between 70 and 100 mg/dL.

Type 1 diabetes. Type 1 diabetes, formerly known as insulin-dependent diabetes, is an autoimmune condition that occurs when the body attacks and destroys the cells (called beta cells) that make insulin. Type 1 diabetes accounts for about 5 to 10 percent of cases. Because type 1 diabetics can no longer make insulin, insulin replacement therapy is essential.

Type 2 diabetes. Type 2 diabetes, formerly known as non-insulin-dependent diabetes, occurs when the body is no longer able to use insulin effectively and gradually becomes resistant to its effects. It is a slowly progressing disease that goes through identifiable stages. In the early stages of diabetes, both insulin and glucose levels are elevated (conditions called hyperinsulinemia and hyperglycemia, respectively). In the later stages, insulin levels are reduced, and blood glucose levels are very elevated. Although few people are aware of this crucial distinction, therapy for type 2 diabetes should be tailored to the stage of the disease.

Glycation and oxidative stress are central to the damage caused by diabetes. Unfortunately, neither of them figures into conventional treatment for diabetes, which is generally concerned only with blood sugar control.

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